Hepatic Vitamin A Concentrations and Association with Infectious Causes of Child Death

Objectives To assess postmortem vitamin A (VA) concentrations in children under 5 years of age and evaluate the association between VA deficiency (VAD) and infectious causes of death (CoD). Study design In this cross-sectional study from the Child Health and Mortality Prevention Surveillance (CHAMPS) Network, liver biopsies collected within 72 hours of death were analyzed from 405 stillbirths and children under 5 years in Kenya and South Africa. Total liver VA (TLVA) concentrations were quantified using ultra-performance liquid chromatography, and cutoffs of ≤0.1 μmol/g, >0.1 to <0.7 μmol/g, ≥0.7 to <1.0 μmol/g, and ≥1.0 μmol/g were used to define VAD, adequate VA status, high VA, and hypervitaminosis A, respectively. CoD were determined by expert panel review. Results Among 366 liver samples with viable extraction, pooled prevalences of VAD, adequacy, high VA, and hypervitaminosis were 34.2%, 51.1%, 6.0%, and 8.7%, respectively. VAD was more common among neonates compared with stillbirths, infants, or children, and among those with low birthweight (LBW), underweight, or stunting (P < .05). When adjusting for site, age, and sex, there was no significant association of VAD with increased infectious CoD (OR 1.9, 95% confidence interval [CI] 0.9, 3.8, P = .073). In stratified analyses, VA deficient boys, but not girls, had an increased risk of infectious CoD (OR 3.4, 95% CI 1.3, 10.3, P = .013). Conclusions Definitive postmortem assessment of VA status identified both VAD and VA excess among children under 5 years of age in Kenya and South Africa. VAD in boys was associated with increased risk of infectious mortality. Our findings may inform a transition from universal VA supplementation (VAS) to targeted strategies in certain countries.


CoD
Causes

ORIGINAL ARTICLES
prophylaxis alleviates the effects of measles, diarrhea, vision problems, ear infections, and subsequent hearing loss.WHO recommends universal VAS with preformed VA at 100 000 IU dose to infants 6-11 months of age and 200 000 IU every 4-6 months to children 12-59 months in settings where prevalence of VAD exceeds 20% or the prevalence of night blindness exceeds 1%. 3 Evidencebased strategies to combat VAD also include early initiation of breastfeeding, timely introduction of VA-rich complementary foods, biofortification, food fortification, and emphasis on infectious disease reduction.Total liver VA concentration (TLVAC) is considered the reference standard for assessing the continuum of VA status from deficiency through excess. 1,12,13However, direct measurement of TLVAC requires liver biopsy, which typically is not feasible in living populations.][16][17][18] Eradication of VAD has been the focus of many public health interventions; however, there is no clear guidance on when to scale back universal VAS and whether VAS should continue in countries with multiple overlapping VA interventions. 18o address these research and programmatic knowledge gaps, we evaluated postmortem liver specimens along with detailed data on cause of death from the Child Health and Mortality Prevention Surveillance (CHAMPS) network to examine definitive VA status.We also sought to quantify the association between VAD and infectious causes of death (CoD) to inform universal VAS strategies.

Data Source
0][21][22][23][24][25][26][27][28] In brief, CHAMPS collects standardized, population-based, surveillance data from sites in Africa and Southern Asia with high child mortality to understand and track preventable CoD.These data include demographic characteristics, extensive postmortem diagnostic results, and data from abstracting clinical medical records.Postmortem tissue samples are secured using minimally invasive tissue sampling (MITS). 20,21,25,27,29Data collection procedures were approved by ethics committees in each CHAMPS site as well as Emory University (Emory IRB#: 00 091 706).Consent for MITS, verbal autopsy, and clinical data abstraction was obtained from parents or guardians.CHAMPS ethical protocols are described in greater detail on the study website (https://champshealth.org/protocols/).This study followed the Strengthening the Reporting of Observational Studies in Epidemiology reporting guideline.

Sample Selection and Exclusions
Liver samples (mean AE SD mass: 19 AE 8 mg) were procured via needle biopsy from 405 stillbirths and cadavers under 5 years within 72 hours of death (median of 19 hours) using standard procedures. 27Multiple biopsies were collected from needle puncture in the mid-axillary line, in 1 of the three last intercostal spaces with some tissue frozen as quickly as possible and remaining samples fixed in 10% neutral buffered formalin for histological evaluation.All samples collected between May 2017 and December 2019 from the CHAMPS Kenyan and South African sites and deposited in the CHAMPS central biorepository were included.Catchment areas in Kenya included Siaya (rural) and Kisumu (urban) and in South Africa included Soweto (urban).VAD (based on serum retinol) is high in Kenya and moderate in South Africa. 30[33] Exposure: Liver VA Concentrations Liver samples were weighed to the nearest 0.001 mg on a Sartorius CP2P scale (range 1-46 mg), extracted with dichloromethane, 34 and TLVACs (retinol and retinyl esters) were quantified using a published ultra-performance liquid chromatographic gradient and calibrated against a purified standard (Sigma) 35 C23-b-apo-carotenol was used as an internal standard to measure and account for extraction efficiency; samples with extraction efficiencies <10% were excluded.The detection limit of the was 0.001 mmol/g for VA esters.Cutoffs for TLVAC of £0.1 mmol/g, >0.1 to <0.7 mmol/g, ³0.7 to <1.0 mmol/g, and ³1.0 mmol/g were used to define VAD, adequate VA status, high VA, and hypervitaminosis A, respectively. 1,36tcome: Infectious CoD The Determination of CoD (DeCoDe) is a process to evaluate multiple CoD and decrease subjectivity, through a standardized approach of applying clinical and laboratory findings to diagnose the conditions contributing to death based on completeness and specificity of data.A complete description of the DeCoDe process has been published elsewhere. 19Briefly, stillbirths and deaths in children <5 years are identified in site catchment areas; following parental consent, MITS are collected and tissues examined using microbiology and pathology techniques.CHAMPS teams also review clinical records and interview parents using a standard verbal autopsy form.All available data for each death are then reviewed by site-specific DeCoDe panels that consist of subject matter experts including pediatricians, obstetricians, epidemiologists, pathologists, and microbiologists.The panels review available case data and determine the chain of events (immediate, underlying, comorbid causes) leading to death using WHO's International Classification of Diseases, 10th Revision and WHO application of International Classification of Diseases, 10th Revision deaths during the perinatal period. 37,38Immediate, underlying, and morbid CoD will subsequently be referred to as those within the causal chain. 19ur primary outcome of interest was all infectious CoDs within the causal chain defined as diarrheal diseases, congenital infections, human immunodeficiency virus, lower respiratory infection (LRI), malaria, measles, meningitis, encephalitis, neonatal sepsis, other infections, rabies, sepsis, syphilis, tuberculosis, or upper respiratory infections in the causal chain.Sub-analyses were performed to examine the association between VAD and infectious CoDs with an established relationship with VA, defined as deaths due to LRI s, sepsis, and diarrheal diseases.

Statistical Analyses
We first developed frequency distributions to describe demographic characteristics stratified by age.Pearson chi-square tests and univariable models were used to examine relationships between covariates, exposure and outcomes when exploring potential confounders.Confounding covariates were also considered if sufficient evidence in existing literature warranted inclusion in the model.
Covariates evaluated as potential effect modifiers and confounders included: age (categorized as stillbirths and deaths in the first 24 hours, neonates [1 through 27 days], infants and children [28 days through 59 months]), site (Kenya, South Africa), and sex (male, female).We also examined locations of death (facility or community).Low birthweight (LBW) was defined as <2500 g.We also examined evidence of malnutrition based on anthropometry at death.Anthropometric measurements were collected during the MITS examination using standard equipment, including wooden heightlength measuring boards (ShorrBoard, Weigh and Measure, LLC) and digital scales (Rice Lake Weighing Systems, Inc).Z-scores for anthropometric indices were produced using the WHO growth standards anthro R package. 39Rigor mortis did not prevent acquisition of accurate anthropometric measurements. 40We examined the individual effects of underweight, stunting, or wasting, as well as any malnutrition defined as the presence of either underweight, wasting, or stunting at death, using z-scores < À2 SD for weight-forlength (wasting), length-for age (stunting), or weight-forage (underweight).
Ordinal logistic regression was used to quantify the relationship between the exposure VAD and all infectious CoD.The reference category for the exposure was adequate VA status.Models assessed for effect modification (P < .01),and if evidence of heterogeneity, stratified analyses were performed.Modeling was repeated with the outcome of select infectious CoD with an established relationship with VAD.Model significance was evaluated using P < .05.Odds ratios (OR) and 95% confidence intervals (95% CI) were reported.Model diagnostics, including Akaike Information Criteria, were considered when selecting final models.All analyses were completed in R statistical software (version 4.2.1,The R Foundation for Statistical Computing). 41

Results
Of the 405 liver samples sent for analysis, 39 were excluded due to identification errors (n = 2), low or missing extraction efficiencies (n = 35), or TLVACs above 3.0 mmol/g (n = 2), which were assumed to be a result of damaged livers due to VA toxicity leaking retinyl esters into the serum. 42The majority of samples analyzed (n = 366, 90.3%) had good extraction efficiencies; 190 (51.9%) were from Kenya and 176 (48.1%) were from South Africa (Figure 1).
Nearly half enrolled children were infants and children (46.7%); 26.5% were stillbirths and deaths in the first 24 hours; and the remaining 26.8% were neonates (Table I).There was an even distribution of sex by age group.There were differences in age distributions by site and location of deaths with infants and children being most common in Kenya, and neonates most common in South Africa.Eight in 10 cases had evidence of malnutrition based on anthropometry at death, and the prevalence of underweight (79.4%) and stunting (69.9%) was significantly higher among neonates.Overall, nearly 2 in 3 deaths were due to infectious CoDs, and prevalence of infectious CoDs was highest among infants and children (90.1%), compared with 66.3% of neonates and only 2.9% of stillbirths or deaths in the first 24 hours (P < .01).
Pooled prevalence of VAD, adequate VA, high VA, and hypervitaminosis was 34.2%, 51.1%, 6.0%, and 8.7%, respectively (Table II).The distribution of TLVACs differed significantly by age but not by site, sex, location of death, wasting, or infectious CoD.VAD was highest in neonates (39.8%) and lowest in infants and children (29.8%).Conversely, high or hypervitaminosis was highest in older children.Cases that were LBW, underweight, stunted, or had any evidence of malnutrition based on anthropometry at death had higher prevalence of VAD.
Crude models examining the association between VAD and infectious CoD were not significant (Figure 2).When adjusting for site, sex, and age, there was no significant association between VAD and increased infectious CoDs (OR 1.9, 95%CI 0.9, 3.8, P = .073).We did, however, note heterogeneity by sex (P = .09),and thus performed stratified analysis.Boys with VAD, but not girls, had a significantly increased risk of mortality due to infectious CoDs (OR boys 3.4, 95%CI 1.3, 10.3, P = .013;OR girls 0.9, 95%CI 0.3, 2.7, P = .905).LBW and indicators of malnutrition at death were either nonsignificant predictors of cause of mortality or did not improve model fit and thus were not included in final models.
Sub-analysis of specific infectious CoDs (LRIs, sepsis, and diarrheal diseases) did not reveal a significant association between VAD and increased mortality due to LRIs, sepsis, and diarrhea (OR: 1.7, 95% CI 1.0, 3.1, P = .06),but showed significant effect modification by sex (P = .02).Similar to the primary outcome of all infectious CoD, boys, but not girls, had a significantly increased risk of death due to LRIs, sepsis, or diarrheal CoDs in the final adjusted model (OR boys 2.9, 95% CI 1.4, 6.7, P = .006;OR girls 0.8, 95% CI 0.3, 1.9, P = .555).Final models were stratified by age group, and VAD was associated with all causes of infectious deaths among stillbirths or deaths in the first 24 hours (OR 8.8, 95% CI 1.3, 176.0) and infants and children (OR 3.8, 95% CI 0.97-25.6),but not among neonates (OR 1.0 95% CI 0.4, 2.4).Sample sizes were too low to assess the association of VAD and mortality due to LRIs, sepsis, and diarrhea stratified by age.

Discussion
This large, multisite study of reference-standard postmortem liver VA concentrations in children under 5 years of age suggests coexistence of VAD and excess in Kenya and South Africa, both settings with ongoing public health interventions designed to prevent VAD (eg, VAS, food fortification).Furthermore, we found increased odds of dying of all infectious CoD as well as LRIs, sepsis, and diarrheal diseases among boys with VAD, but not among girls.
WHO defines VAD as a severe public health problem if the national prevalence of serum retinol <0.7 mmol/L in PSC exceeds 20%. 1 According to the latest national nutrition survey in South Africa in 2012, the prevalence of VAD among PSC was 44%. 43The 2011 Kenya National Micronutrient Survey found 9.2% of PSC with VAD, but 52.6% of PSC had marginal VAD (serum retinol: 0.7-1.05mmol/L) and thus were at risk of becoming deficient. 44The Micronutrient Forum recommends that countries complete a micronutrient survey every 5 years to track changes in status and to inform national nutrition programs. 455][16][17][18] Commonly used biomarkers of VA status, including serum retinol and RBP concentrations, are subject to limitations in both clinical and public health settings.Serum retinol is homeostatically controlled and does not decrease until liver reserves of VA are depleted.Additionally, both retinol and RBP decrease in the presence of inflammation or infection, which can contribute to overestimation of VAD. 46Both RBP and serum retinol may miss excess or toxic levels of VA, which may be helpful in calibrating VA programs.The utility of assessing TLVAC within mortality surveillance as a more reliable tool for monitoring population VA status warrants additional research.
The observed coexistence of VAD and VA excess may be present due to various factors including dietary intake, poverty, food insecurity, 47,48 cultural perceptions around food, 49 and access to health services.Both Kenya and South Africa have mandatory staple food VA fortification programs (vegetable fats and oil in Kenya and wheat and maize flour in South Africa) as well as universal biannual VAS among 6-59 month olds 33,50 ; however, VAS coverage varies between 30-80% in Kenya and 30-40% in South Africa.Incomplete and duplicative VAS coverage may explain the coexistence of deficiency and excess in the same population. 48,51In 1 area of South Africa, the number of capsules received through VAS was directly related to increasing liver reserves. 52Across five African countries, both deficiency and excessive stores of VA have been documented. 53n Kenya, the latest Demographic and Health Survey data suggest that 3 in 4 children under 2 years of age receive VArich food sources as well as VAS, which may help contextualize the adequate to high VA levels in nearly two-thirds of children. 54In South Africa, traditional beliefs around appropriate foods during pregnancy and early life may contribute to both deficiency and excess VA.For example, in the Northern Cape province of South Africa where sheep farming is a main agricultural activity, 41-70% of children 12-23 months of age consume liver, an exceptionally high source of preformed VA 32,55 ; whereas limited consumption of orange color, VA rich plant-based foods and meat occurs during pregnancy for fear of adverse or undesirable traits in the baby, which may contribute to VAD. 49 Therefore, the coexistence of VAD and excess in Kenya and South Africa may be attributed to a complex interplay of poverty, food insecurity, cultural food practices and beliefs, and overlapping VA interventions.
VADhas a significant impact on U5M, and studies have shown that VA deficient children are more susceptible to infections, such as measles, diarrhea, and respiratory diseases [6][7][8][9] and are therefore at greater risk of U5M.Inadequate intake of VA can weaken the immune system, Weight-for-age (WAZ), length/height-for-age (LAZ), and weight-for-length/height (WLZ) z-scores <2 SD was used to define underweight, stunted, and wasted, respectively.Sample decrease within the underweight category due to 3 cases missing weight, 1 case missing age in days, and 1 case with WAZ outside of defined limits.Sample decrease within the stunted category due to 20 cases missing z-score due to lengths under 45 cm and 5 cases with LAZ outside of defined limits (refer to methods section).Sample decrease within the wasting category due to 117 cases missing z-score due to lengths under 45 cm, 3 cases with missing weight, 3 cases outside of the defined upper limit, and 1 case with outside the measurement limits for raw length captured by the WHO-GS.Differences in sample size for wasting and stunting exist because LAZ is estimable based on length according to completed age and sex, whereas wasting is a measure of weight by length, details on the WHO-GS can be referenced elsewhere. 41ny malnutrition was defined WAZ, LAZ, or WLZ < -2 SD at death.Sample size drop in any malnutrition based on anthropometry at death due to 1 measurement outside of the WHO-GS bounds, and 7 cases with z-scores outside of the limits captured by the WHO-GS.All Infectious diseases deaths included: diarrheal diseases, congenital infections, HIV, lower respiratory infections, malaria, measles, meningitis/encephalitis, neonatal sepsis/sepsis, other infections, rabies, syphilis, tuberculosis, or upper respiratory infections in the causal chain.Sub-analyses were conducted to investigate the association between vitamin A deficiency and select infectious causes of death with an established relationship with vitamin A. These conditions included: included: lower respiratory infections, neonatal sepsis/sepsis, and diarrheal diseases.*n (%).†Pearson's Chi-squared tests examining frequency distributions of demographic characteristics by age group.‡Birthweight was abstracted from maternal or child clinical records.For deaths and stillbirths in the first 24 hours, if clinical abstraction data was missing, birthweight was assumed to be the MITS weight.Low birthweight was defined as <2500 g.Eighty-seven cases missing clinical abstraction data from maternal and child clinical records; 1 stillbirth or death in the first 24 hours was missing both clinical abstraction weight and MITS weight.
making children more susceptible to illnesses that lead to death.The complex interplay between VA, infection, and mortality 56 may elucidate the mechanisms by which children with VAD in our study were found to have elevated odds, although not significant, of dying from an infectious disease.Our study also suggests that the effects of VAD on U5M may vary by sex.This finding complements existing literature that suggests that boys have a higher U5M than girls in many low and middle-income countries, and that VASin early infancy may have more beneficial effects on mortality for males than for females. 57Further highpowered research is needed to better understand sex differences in requirements for VA, factors associated with sex inequality in U5M, and the impacts of targeted interventions and management of selective threats to male survival including prematurity and early childhood infection. 58uture studies may consider replication of this study across all CHAMPS sites.This study has several strengths.First, this study is innovative in its use of postmortem liver samples to conduct reference-standard VA assessment through MITS.The MITS technique is a low-cost, nondisfiguring, needle-based approach to acquire postmortem samples.Previous studies have shown that MITS samples are highly correlated with complete diagnostic autopsies. 21Additionally, previous research on the acceptability and feasibility of this approach with community participants found that not only did families consent to MITS at higher than anticipated rates (75%), but an overwhelming majority of parents expressed relief and gratitude for being provided information about why their child died. 20,21,25,29Second, this is a large and recent assessment of TLVACs using postmortem livers.While previous studies have utilized postmortem liver specimens for reference-standard VA assessment, these early studies often lacked sufficient sample size, failed to have representation from the first 5 years of life, and lacked data from countries with high U5M rates. 15,16,59Third, the timeliness of specimen collection is a key strength of our study.Previous literature has shown that postmortem liver is viable up to 108 hours after death.Our samples were collected within 72 hours after death.
Our study has limitations.First, the cross-sectional nature of our data does not allow inference of causality.While certain infections themselves may cause VADdue Weight-for-age (WAZ), length/height-for-age (LAZ), and weight-for-length/height (WLZ) z-scores <2 SD was used to define underweight, stunted, and wasted, respectively.Sample decrease within the underweight category due to 3 cases missing weight, 1 case missing age in days, and 1 case with WAZ outside of defined limits.Sample decrease within the stunted category due to 20 cases missing z-score due to lengths under 45 cm and 5 cases with LAZ outside of defined limits (refer to methods section).Sample decrease within the wasting category due to 117 cases missing z-score due to lengths under 45 cm, 3 cases with missing weight, 3 cases outside of the defined upper limit, and 1 case with outside the measurement limits for raw length captured by the World Health Organization growth standards (WHO-GS).Differences in sample size for wasting and stunting exist because LAZ is estimable based on length according to completed age and sex, whereas wasting is a measure of weight by length, details on the WHO-GS can be referenced elsewhere. 41ny malnutrition was defined WAZ, LAZ, or WLZ < -2 SD.Sample size drop in any malnutrition based on anthropometry at death due to 1 measurement outside of the WHO-GS bounds, and 7 cases with z-scores outside of the limits captured by the WHO-GS.All Infectious diseases deaths included: diarrheal diseases, congenital infections, HIV, lower respiratory infections, malaria, measles, meningitis/encephalitis, neonatal sepsis/sepsis, other infections, rabies, syphilis, tuberculosis, or upper respiratory infections in the causal chain.Sub-analyses were conducted to investigate the association between vitamin A deficiency and infectious causes of death with an established relationship with vitamin A. These conditions included: lower respiratory infections, neonatal sepsis/sepsis, and diarrheal diseases.*Vitamin A status was defined using cutoffs of <0.1 mmol/g, ³0.1 to <0.7 mmol/g, ³0.7 to <1.0 mmol/g, and ³1.0 mmol/g to indicate VAD, adequate VA status, high VA, and hypervitaminosis, respectively. 1earson's Chi-squared tests examining frequency distributions of demographic characteristics by Vitamin A Status. ‡n (%).§Birthweight was abstracted from maternal or child clinical records.For deaths and stillbirths in the first 24 hours, if clinical abstraction data was missing, birthweight was assumed to be the MITS weight.Low birthweight was defined as <2500 g.Eighty-seven cases missing clinical abstraction data from maternal and child clinical records; 1 stillbirth or death in the first 24 hours was missing both clinical abstraction weight and MITS weight.
to increased nutrient utilization or losses, our analyses were informed by the presumed causality of VAD and infectious mortality, as confirmed by both biology and prior randomized clinical trials.Further, the association between VAD and infectious CoD was consistent across age groups, even in stillbirths or deaths in the first 24 hours who likely had in utero VAD due to poor VA supply in pregnancy rather than acquiring it from an infection.Second, we lack data on dietary patterns, fortification coverage, and history of VAS that may be helpful to contextualize the coexistence of deficiency and excess in our sample.Third, we cannot control the variability of antemortem data; eg, data on VAS from child clinical abstraction was either missing or unknown for most of our samples.Further, due to lack of availability of data we were not able to explore the impact of poverty and other sociodemographic factors in our models.Fourth, the size of the liver sample was limited and duplicate analysis could not be performed, which would have been the case for low extraction efficiencies.Degradation of VA in liver also could have impacted samples with delayed collection after death, as could potential differences in VA from liver samples collected from different lobes.Finally, CHAMPS is an ongoing surveillance system and is refined through lessons learned through network sharing and in-person process monitoring.This means that results and conclusions using these data can change over time.
A unique challenge facing policy makers will be determining the appropriate balance of VA interventions, as deficiency and excess may coexist in the same population or differ among various subgroups.There is a continued need for routine population-based assessment of micronutrient status that includes dietary data, reliable  *Deaths may have multiple conditions in the causal pathway (eg, underlying, immediate, and antecedent), therefore the number of causes of death could exceed the number of deaths (and the sum would be >100%).

ORIGINAL ARTICLES
Hepatic Vitamin A Concentrations and Association with Infectious Causes of Child Death biological indicators of VA status including TLVAC as a data source, 60,61 and consumption patterns of industrially fortified VA staple foods.Together, these data may be used to inform future changes to universal VAS strategies, including a transition from universal VAS to targeted strategies in certain countries.n

Declaration of Competing Interest
This work was funded by grant OPP1126780 from the Bill & Melinda Gates Foundation and a seed grant from the Global Health Institute at University of Wisconsin-Madison.The funders participated in discussions of study design and data collection.They did not participate in the conduct of the study; the management, analysis, or interpretation of the data; preparation, review, or approval of the manuscript; or decision to submit the manuscript for publication.
The authors declare no conflicts of interest.

Figure 1 .
Figure 1.Study profile of children under 5 years with analyzed liver specimens from CHAMPS Kenya and South Africa Sites.

Figure 2 .
Figure 2. Crude and adjusted models of the association between vitamin A deficiency and odds of dying of infectious causes of death among children under 5 years with analyzed liver specimens from CHAMPS Kenya and South Africa Sites, n = 312 children.The crude model depicts the unadjusted relationship between vitamin A deficiency and infectious causes of death.Adjusted models depict the relationship between vitamin A deficiency and infectious causes of death controlling for site, age, and sex.Box A. All causes of infectious deaths defined as deaths due to diarrheal diseases, congenital infections, HIV, lower respiratory infection, malaria, measles, meningitis/encephalitis, sepsis, other infections, rabies, syphilis, tuberculosis, or upper respiratory infection in the causal chain.Box B. Sub-analysis of the most common causes of infectious disease mortality which have an established relationship with vitamin A deficiency.These conditions included lower respiratory infection, sepsis, and diarrheal diseases.

Table I .
Demographic characteristics of children under 5 Years (n = 366) with analyzed liver specimens from CHAMPS Kenya and South Africa sites by age group

Table II .
Vitamin A status by demographic characteristics of children under 5 years (n = 366) with analyzed liver specimens from CHAMPS Kenya and South Africa sites

Table III .
Top infectious and noninfectious causes of death by age group among children under 5 years (n = 366) with analyzed liver specimens from CHAMPS Kenya and South Africa sites